Biomedical subjects

Grace Y Sun

Publications and source records attributed to Grace Y Sun.

At least 37 records · Page 2Linked to original sources

PubMed2004

Effect of exercise on postprandial lipemia following a higher calorie meal in Yucatan miniature swine.

Exercise has been shown to attenuate the postprandial lipemic (PPL) response to a modest kcal high-fat meal in numerous human studies, but has not been fully examined in swine. In addition, the effects of exercise on a high-fat meal of larger magnitude have not been examined in humans or in swine. Thus, the purpose of this study was to examine the PPL response to a single, high-fat/cholesterol (HFC) meal (approximately 3,000 kcal, 1,300 kcal from fat) and determine if exercise attenuates the PPL response. Sedentary, female Yucatan miniature swine (n = 10) completed 3 PPL trials: (1) pre diet (PRE); (2) post HFC diet (POST); and (3) post HFC diet plus exercise (EX, 45 minutes at 75% heart rate maximum). Blood samples were collected before (0 hour) and at 2, 4, 6, and 8 hours after the single HFC meal for PPL analysis. Postheparin lipoprotein lipase (LPL) activity was assessed at 8 hours. While fasting LPL activity was significantly increased with the HFC diet, the PPL response to the HFC meal did not differ depending on diet. Furthermore, the PPL response was not significantly altered with a single session of exercise, perhaps because of the severity of the HFC meal, the sedentary nature of the swine, or because LPL activity was not elevated after exercise. These findings suggest that administration of a HFC meal of this magnitude (approximately 3,000 kcal, 1,300 kcal from fat) will promote significant elevations in postprandial triglyceride (TG) concentrations, overwhelm the adaptive response to a HFC diet (elevated LPL activity), and attenuate the beneficial effects of a single exercise session on this system.

Animals↗

PubMed2004

Exercise plus n-3 fatty acids: additive effect on postprandial lipemia.

The purpose of this study was to examine changes in postprandial lipemia (PPL) in recreationally active males following aerobic exercise, omega-3 fatty acids (n-3FA) supplementation, and the combination of the two. PPL following a high-fat meal was measured in 10 recreationally active males (25 +/-1.5 years) under each of the following conditions: no exercise and no n-3 FA supplementation (control); exercise and no n-3FA supplementation (exercise); n-3FA supplementation and no exercise (n-3FA); and exercise and n-3 FA supplementation (combined). Blood was collected before the high-fat meal and at 2, 4, 6, and 8 hours after the meal to assess the PPL response. Supplementation consisted of 4.0 g of n-3FA per day for 5 weeks. Triglyceride (TG) peak response, the total area under the TG curve (TG-AUCT), and the incremental area under the TG curve (TG-AUCI) were used to define the PPL response. TG peak response was significantly reduced 38% by n-3FA supplementation and 50% by the combination of exercise and n-3FA supplementation. N-3FAs significantly reduced the TG-AUCT by 27% and by 42% when combined with exercise. When compared with the exercise trial, the TG-AUCT during the combined trial was significantly lower. Exercise, n-3FAs, and the combination significantly reduced the TG-AUCI by 40%, 42%, and 58%, respectively. These results suggest that the combination of exercise and n-3FA supplementation reduce PPL to a greater degree in recreationally active males when compared with the individual treatments.

Adult↗

PubMed2004

Chronic ethanol-induced subtype- and subregion-specific decrease in the mRNA expression of metabotropic glutamate receptors in rat hippocampus.

BACKGROUND: Chronic ethanol consumption is known to induce adaptive changes in the hippocampal glutamatergic transmission and alter NMDA receptor binding and subunit expression. Metabotropic glutamate (mGlu) receptors have been shown to function as modulators of neuronal excitability and can fine tune glutamatergic transmission. This study was aimed to determine whether chronic ethanol treatment could change the messenger RNA (mRNA) expression of mGlu receptors in the hippocampus. METHODS: Male Sprague Dawley rats were fed a Lieber-DeCarli liquid diet with 5% (w/v) ethanol or isocaloric amount of maltose for 2 months. Quantitative in situ hybridization was carried out using coronal brain sections through the hippocampus. RESULTS: The results revealed decreases in mRNA expression of several mGlu receptors in different subregions of the hippocampus. In the dentate gyrus, mGlu3 and mGlu5 receptor mRNA levels were significantly lower in the ethanol-treated rats than in the control rats. In the CA3 region, the mRNA expression of mGlu1, mGlu5, and mGlu7 receptors showed substantial decreases after ethanol exposure. The mGlu7 receptor mRNA levels were also declined in the CA1 region and the polymorph layer of the dentate gyrus. No changes were found in mRNA expression of mGlu2, mGlu4, and mGlu8 receptors. CONCLUSIONS: Considering the involvement of hippocampal mGlu receptors in learning and memory processes as well as in neurotoxicity and seizure production, the reduced expression of these receptors might contribute to ethanol withdrawal-induced seizures and also may play a role in cognitive deficits and brain damage caused by long-term ethanol consumption.

Animals↗

PubMed2004

Induction of secretory phospholipase A2 in reactive astrocytes in response to transient focal cerebral ischemia in the rat brain.

Although mRNA expression of group IIA secretory phospholipase A2 (sPLA2-IIA) has been implicated in responses to injury in the CNS, information on protein expression remains unclear. In this study, we investigated temporal and spatial expression of sPLA2-IIA mRNA and immunoreactivity in transient focal cerebral ischemia induced in rats by occlusion of the middle cerebral artery. Northern blot analysis showed a biphasic increase in sPLA2-IIA mRNA expression following 60-min of ischemia-reperfusion: an early phase at 30 min and a second increase at a late phase ranging from 12 h to 14 days. In situ hybridization localized the early-phase increase in sPLA2-IIA mRNA to the affected ischemic cortex and the late-phase increase to the penumbral area. Besides sPLA2-IIA mRNA, glial fibrillary acidic protein (GFAP) and cyclo-oxygenase-2 mRNAs, but not cytosolic PLA2, also showed an increase in the penumbral area at 3 days after ischemia-reperfusion. Immunohistochemistry of sPLA2-IIA indicated positive cells in the penumbral area similar to the GFAP-positive astrocytes but different from the isolectin B4-positive microglial cells. Confocal microscopy further confirmed immunoreactivity of sPLA2-IIA in reactive astrocytes but not in microglial cells. Taken together, these results demonstrate for the first time an up-regulation of the inflammatory sPLA2-IIA in reactive astrocytes in response to cerebral ischemia-reperfusion.

Animals↗

PubMed2004

P2Y receptors activate neuroprotective mechanisms in astrocytic cells.

Mechanical or ischemic trauma to the CNS causes the release of nucleotides and other neurotransmitters into the extracellular space. Nucleotides can activate nucleotide receptors that modulate the expression of genes implicated in cellular adaptive responses. In this investigation, we used human 1321N1 astrocytoma cells expressing a recombinant P2Y2 receptor to assess the role of this receptor in the regulation of anti-apoptotic (bcl-2 and bcl-xl) and pro-apoptotic (bax) gene expression. Acute treatment with the P2Y2 receptor agonist UTP up-regulated bcl-2 and bcl-xl, and down-regulated bax, gene expression. Activation of P2Y2 receptors was also coupled to the phosphorylation of cyclic AMP responsive element binding protein that positively regulates bcl-2 and bcl-xl gene expression. Cyclic AMP responsive element decoy oligonucleotides markedly attenuated the UTP-induced increase in bcl-2 and bcl-xl mRNA levels. Activation of P2Y2 receptors induced the phosphorylation of the pro-apoptotic factor Bad and caused a reduction in bax/bcl-2 mRNA expression ratio. All these signaling pathways are known to be involved in cell survival mechanisms. Using cDNA microarray analysis and RT-PCR, P2Y2 receptors were found to up-regulate the expression of genes for neurotrophins, neuropeptides and growth factors including nerve growth factor 2; neurotrophin 3; glia-derived neurite-promoting factor, as well as extracellular matrix proteins CD44 and fibronectin precursor--genes known to regulate neuroprotection. Consistent with this observation, conditioned media from UTP-treated 1321N1 cells expressing P2Y2 receptors stimulated the outgrowth of neurites in PC-12 cells. Taken together, our results suggest an important novel role for the P2Y2 receptor in survival and neuroprotective mechanisms under pathological conditions.

Animals↗

PubMed2003

Phospholipase A2 in the central nervous system: implications for neurodegenerative diseases.

Phospholipase A2 (PLA2) belongs to a family of enzymes that catalyze the cleavage of fatty acids from the sn-2 position of phospholipids. There are more than 19 different isoforms of PLA2 in the mammalian system, but recent studies have focused on three major groups, namely, the group IV cytosolic PLA2, the group II secretory PLA2 (sPLA2), and the group VI Ca(2+)-independent PLA2. These PLA2s are involved in a complex network of signaling pathways that link receptor agonists, oxidative agents, and proinflammatory cytokines to the release of arachidonic acid (AA) and the synthesis of eicosanoids. PLA2s acting on membrane phospholipids have been implicated in intracellular membrane trafficking, differentiation, proliferation, and apoptotic processes. All major groups of PLA2 are present in the central nervous system (CNS). Therefore, this review is focused on PLA2 and AA release in neural cells, especially in astrocytes and neurons. In addition, because many neurodegenerative diseases are associated with increased oxidative and inflammatory responses, an attempt was made to include studies on PLA2 in cerebral ischemia, Alzheimer's disease, and neuronal injury due to excitotoxic agents. Information from these studies has provided clear evidence for the important role of PLA2 in regulating physiological and pathological functions in the CNS.

Alzheimer Disease↗

PubMed2003

Oxidant-mediated AA release from astrocytes involves cPLA(2) and iPLA(2).

Excessive generation of reactive oxygen species (ROS) in the central nervous system (CNS) is a leading cause of neuronal injury. Despite yet unknown mechanisms, oxidant compounds such as H(2)O(2) have been shown to stimulate the release of arachidonic acid (AA) in a number of cell systems. In this study, H(2)O(2) and menadione, a compound known to release H(2)O(2) intracellularly, were used to examine the phospholipases A(2) (PLA(2)) responsible for AA release from primary murine astrocytes. Both H(2)O(2) and menadione dose-dependently stimulated AA release, and the release mediated by H(2)O(2) was completely inhibited by catalase. H(2)O(2) also stimulated phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A(2) (cPLA(2)). However, complete inhibition of cPLA(2) phosphorylation by U0126, an inhibitor for mitogen-activated protein kinase kinase (MEK) and GF109203x, a nonselective PKC inhibitor preferring the conventional and novel isoforms, only reduced H(2)O(2)-stimulated AA release by 50%. MAFP, a selective, active, site-directed, irreversible inhibitor of both cPLA(2) and the Ca(2+)-independent iPLA(2), nearly completely inhibited H(2)O(2)-mediated AA release; but, HELSS, a potent irreversible inhibitor of iPLA(2), only inhibited H(2)O(2)-mediated AA release by 40%. Along with the observation that H(2)O(2)-mediated AA release was only partially inhibited upon chelating intracellular Ca(2+) by BAPTA, these results indicate the involvement of both cPLA(2) and iPLA(2) in H(2)O(2)-mediated AA release in murine astrocytes.

Animals↗

PubMed2003

Cholesterol distribution in the Golgi complex of DITNC1 astrocytes is differentially altered by fresh and aged amyloid beta-peptide-(1-42).

The Golgi complex plays an important role in cholesterol trafficking in cells, and amyloid beta-peptides (Abetas) alter cholesterol trafficking. The hypothesis was tested that fresh and aged Abeta-(1-42) would differentially modify Golgi cholesterol content in DINTC1 astrocytes and that the effects of Abeta-(1-42) would be associated with the region of the Golgi complex. Two different methods were used to determine the effects of Abeta-(1-42) on Golgi complex cholesterol. Confocal microscopy showed that fresh Abeta-(1-42) significantly increased cholesterol and that aged Abeta-(1-42) significantly reduced cholesterol content in the Golgi complex. Isolation of the Golgi complex into two fractions using density gradient centrifugation showed effects of aged Abeta-(1-42) similar to those observed with confocal microscopy but revealed the novel finding that fresh Abeta-(1-42) had opposite effects on the two Golgi fractions suggesting a specificity of Abeta-(1-42) perturbation of the Golgi complex. Phosphatidylcholine-phospholipase D activity, cell membrane cholesterol, and apolipoprotein E levels were associated with effects of fresh Abeta-(1-42) on cholesterol distribution but not with effects of aged Abeta-(1-42), arguing against a common mechanism. Extracellular Abeta-(1-42) targets the Golgi complex and disrupts cell cholesterol homeostasis, and this action of Abeta-(1-42) could alter cell functions requiring optimal levels of cholesterol.

Amyloid beta-Peptides↗

PubMed2003

Extracellular signal-regulated kinase 2 mRNA expression in the rat brain during aging.

Aging is accompanied by the loss of memory and cognitive functions. The extracellular signal-regulated kinase (ERK) pathway has been shown to play an essential role in synaptic plasticity and memory. Although a reduction in basal ERK1/2 activity has been found in the cerebral cortex in aged rats, changes in ERK1/2 mRNA expression during aging have not been described. In this study, we investigated age differences in the mRNA expression of ERK2 in different brain regions of male Fisher 344 rats (three age-groups) using quantitative in situ hybridization. No age-dependent changes in ERK2 mRNA were detected in the cerebellum or cortical areas. However, in the hippocampus, a 20% decline in mRNA levels was observed in the CA3 region in the 12-month-old group as compared to the 3-month-old group. These results suggest that the impairment in ERK1/2 activity observed during aging is probably not regulated at the gene expression level.

Aging↗

PubMed2003

P2X7 nucleotide receptor activation enhances IFN gamma-induced type II nitric oxide synthase activity in BV-2 microglial cells.

Under normal and pathological conditions, brain cells release nucleotides that regulate a wide range of cellular responses due to activation of P2 nucleotide receptors. In this study, the effect of extracellular nucleotides on IFN gamma-induced NO release in murine BV-2 microglial cells was investigated. BV-2 cells expressed mRNA for metabotropic P2Y and ionotropic P2X receptors. Among the P2 receptor agonists tested, ATP, ADP, 2',3'-O-(4-benzoylbenzoyl)-ATP (BzATP), and 2-methylthio-ATP (2-MeSATP), but not UTP, enhanced IFN gamma-induced iNOS expression and NO production, suggesting that the uridine nucleotide receptors P2Y2 and P2Y6 are not involved in this response. U0126, an antagonist for MEK1/2, a kinase that phosphorylates the extracellular signal-regulated kinases ERK1/2, decreased IFN gamma-induced NO production. BzATP, a potent P2X7 receptor agonist, was more effective than ATP, ADP, or 2-MeSATP at enhancing IFN gamma-induced ERK1/2 phosphorylation. Consistent with activation of the P2X7 receptor, periodate-oxidized ATP, a P2X7 receptor antagonist, and suramin, a non-specific P2 receptor antagonist, inhibited the effect of ATP or BzATP on IFN gamma-induced NO production, whereas pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), an antagonist of several P2X receptor subtypes, was ineffective. These results suggest that activation of P2X7 receptors may contribute to inflammatory responses in microglial cells seen in neurodegenerative diseases.

Adenosine Diphosphate↗

PubMed2003

Mechanisms of P2X7 receptor-mediated ERK1/2 phosphorylation in human astrocytoma cells.

Astrocytes are involved in normal and pathological brain functions, where they become activated and undergo reactive gliosis. Astrocytes have been shown to respond to extracellular nucleotides via the activation of P2 receptors, either G protein-coupled P2Y receptors or P2X receptors that are ligand-gated ion channels. In this study, we have examined the manner in which activation of the P2X(7) nucleotide receptor, an extracellular ATP-gated ion channel expressed in astrocytes, can lead to the phosphorylation of ERK1/2. Results showed that the P2X(7) receptor agonist 2',3'-O-(4-benzoyl)benzoyl-ATP induced ERK1/2 phosphorylation in human astrocytoma cells overexpressing the recombinant rat P2X(7) receptor (rP2X(7)-R), a response that was inhibited by the P2X(7) receptor antagonist, oxidized ATP. Other results suggest that rP2X(7)-R-mediated ERK1/2 phosphorylation was linked to the phosphorylation of the proline-rich/Ca(2+)-activated tyrosine kinase Pyk2, c-Src, phosphatidylinositol 3'-kinase, and protein kinase Cdelta activities and was dependent on the presence of extracellular Ca(2+). These results support the hypothesis that the P2X(7) receptor and its signaling pathways play a role in astrocyte-mediated inflammation and neurodegenerative disease.

Astrocytes↗

PubMed2002

Resveratrol protects against global cerebral ischemic injury in gerbils.

Increased oxidative stress has been implicated in the mechanisms of delayed neuronal cell death (DND) following cerebral ischemic insult. In this study, we investigated whether resveratrol, a polyphenolic antioxidant enriched in grape, may ameliorate ischemia-induced neuron cell death. Mongolian gerbils were divided into three groups, namely, sham control, ischemia and ischemia treated with resveratrol. Transient global cerebral ischemia was induced by occlusion of both common carotid arteries (CCA) for 5 min. Resveratrol was injected i.p. (30 mg/kg body weight), either during or shortly after CCA occlusion, and again at 24 h after ischemia. Cerebral blood flow was monitored before and during CCA occlusion using a laser Doppler flowmeter. Brain sections were immuno-stained for neurons, astrocytes and microglial cells. A time course study was also carried out to assess the bioavailability of resveratrol in serum, liver and brain using high performance liquid chromatography (HPLC). Morphometric measurements indicated extensive DND in the hippocampal CA1 region 4 days after ischemia and that neuron cell death was marked by the increase in reactive astrocytes and microglial cells. Administration of resveratrol, either during or after CCA occlusion, significantly (P<0.05) decreased DND as well as glial cell activation. Analysis of resveratrol after i.p. injection indicated its presence in serum, liver and brain with peak activity at 1, 4 and 4 h, respectively. This study demonstrated for the first time that resveratrol, a polyphenolic antioxidant, can cross the blood-brain barrier and exert protective effects against cerebral ischemic injury.

Animals↗

PubMed2002

The "French Paradox" and beyond: neuroprotective effects of polyphenols.

Chronic ethanol ingestion is known to cause oxidative damage to a number of organs including the brain. This is partly due to the ability of ethanol to enhance oxygen free radical production and lipid peroxidation. Increase in oxidative stress has been regarded as an important underlying factor for a number of human health problems including cardiovascular diseases, aging, as well as many age-related neurodegenerative diseases. The strikingly low incidences of coronary heart diseases (CHD) in France, despite intake of a high-fat diet, have been attributed to the consumption of red wine containing high levels of polyphenolic compounds. In recent years, understanding the "French Paradox" has stimulated new research interest to investigate whether polyphenolic antioxidants may offer protective effects beyond the cardiovascular system, and whether polyphenols from other botanical sources may similarly offer beneficial effects to human health. Our studies with animal models have provided information clearly indicating the ability of grape polyphenols to ameliorate neuronal damages due to chronic ethanol consumption. Studies with resveratrol, an important component of grape polyphenols, also show protective effects on neuron cell death induced by ethanol and other oxidative agents. These studies demonstrate an urgent need to extend research beyond the "French Paradox" towards better understanding molecular mechanisms of action of polyphenolic compounds and their application to human health.

Antioxidants↗

PubMed2002

A new role for apolipoprotein E: modulating transport of polyunsaturated phospholipid molecular species in synaptic plasma membranes.

Phospholipids and their acyl group composition are important in providing the proper membrane environment for membrane protein structure and function. In particular, the highly unsaturated phospholipids in synaptic plasma membranes in the CNS are known to play an important role in modulating receptor function and neurotransmitter release processes. Apolipoprotein E (apoE) is a major apolipoprotein in the CNS, mediating the transport of cholesterol, phospholipids and their fatty acids, particularly in reparative mechanisms during neuronal injury. This study was performed to determine whether deficiency in the apoE gene contributes to an alteration of the phospholipids in synaptic plasma membranes. Phospholipid molecular species were identified and quantitated by HPLC/electrospray ionization-mass spectrometry. Analysis of the different phospholipid classes in membranes of apoE-deficient and C57BL/6 J mice indicated no obvious differences in the distribution of different phospholipid classes but substantial differences in composition of phospholipid molecular species. Of special interest was the prevalence of phospholipids (phosphatidylcholine, diacyl-phosphatidylethanolamine, and phosphatidylserine) with 22:6n-3 in both the sn-1 and sn-2 positions of SPM and these phospholipid species were significantly higher in apoE-deficient mice as compared to control mice. Since polyunsaturated fatty acids in neurons are mainly supplied by astrocytes, these results revealed a new role for apoE in regulating polyunsaturated phospholipid molecular species in neuronal membranes.

Alzheimer Disease↗

PubMed2002

Role of PKC and MAPK in cytosolic PLA2 phosphorylation and arachadonic acid release in primary murine astrocytes.

Although Group IV cytosolic phospholipase A2 (cPLA2) in astrocytes has been implicated in a number of neurodegenerative diseases, mechanisms leading to its activation and release of arachidonic acid (AA) have not been clearly elucidated. In primary murine astrocytes, phorbol myristate acetate (PMA) and ATP stimulated phosphorylation of ERK1/2 and cPLA2 as well as evoked AA release. However, complete inhibition of phospho-ERK by U0126, an inhibitor of mitogen-activated protein kinase kinase (MEK), did not completely inhibit PMA-stimulated cPLA2 and AA release. Epidermal growth factor (EGF) also stimulated phosphorylation of ERK1/2 and cPLA2[largely through a protein kinase C (PKC)-independent pathway], but EGF did not evoke AA release. These results suggest that phosphorylation of cPLA2 due to phospho-ERK is not sufficient to evoke AA release. However, complete inhibition of ATP-induced cPLA2 phosphorylation and AA release was observed when astrocytes were treated with GF109203x, a general PKC inhibitor, together with U0126, indicating the important role for both PKC and ERK in mediating the ATP-induced AA response. There is evidence that PMA and ATP stimulated AA release through different PKC isoforms in astrocytes. In agreement with the sensitivity of PMA-induced responses to PKC down-regulation, prolonged treatment with PMA resulted in down-regulation of PKCalpha and epsilon in these cells. Furthermore, PMA but not ATP stimulated rapid translocation of PKCalpha from cytosol to membranes. Together, our results provided evidence for an important role of PKC in mediating cPLA2 phosphorylation and AA release in astrocytes through both ERK1/2-dependent and ERK1/2-independent pathways.

Adenosine Triphosphate↗

PubMed2002

Exercise training does not reduce hyperlipidemia in pigs fed a high-fat diet.

The pig is often used as a model for studying lipoprotein metabolism as it relates to human atherosclerosis, but few studies have examined the complete lipoprotein profile and related enzymes in swine ingesting an atherogenic diet. We examined whether exercise training would moderate the effects of an atherogenic diet on lipoproteins and lipoprotein lipase (LPL) activity in miniature swine. Male (n = 30) and female (n = 32) swine were initially divided into 2 dietary groups: one consumed low-fat (8%) pig chow, and one consumed pig chow supplemented with 2% cholesterol, 17.1% coconut oil, 2.3% corn oil, and.7% sodium cholate (46% kcal from fat). Following 30 days on the diets, pigs from each diet group were further divided into sedentary and exercise trained subgroups, each cell with 6 to 8 pigs. Training occurred 5 days per week on a treadmill in which the intensity and duration were progressively increased during the 16- to 20-week training period to 75 minutes of aerobic running per session. A 4-way analysis of variance (ANOVA) with repeated measures on time indicated that at the conclusion of the study the atherogenic diet caused significantly (P <.05) increased cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and subfractions, low-density lipoprotein cholesterol (LDL-C) and subfractions, and LPL activity in both genders. For cholesterol, TG, HDL-C, HDL(2)-C, LDL-C, LDL(1&2)-C, and hepatic lipase, the female response to the diet was exaggerated compared to the male response. Exercise training produced no group differences or interactions on any lipoprotein variable. These results suggest that an atherogenic diet has a greater impact on the lipoproteins of female miniature swine than males. Furthermore, under the conditions of this study, exercise training does not moderate the effects of an atherogenic diet on lipoproteins.

Animals↗

PubMed2002

Changes in LPLa and reverse cholesterol transport variables during 24-h postexercise period.

We investigated the time course of exercise-induced lipoprotein lipase activity (LPLa) and reverse cholesterol transport (RCT) during the 24-h postexercise period. Subjects were 10 sedentary normolipidemic males [NTG; fasting triglyceride (TG) = 89.1 +/- 8.6 mg/dl] and 6 hyperlipidemic males (HTG; fasting TG = 296.8 +/- 64.0 mg/dl). Each subject performed a control trial (no exercise) and 4 exercise trials. In the exercise trials, a subject jogged on a treadmill at 60% of his maximal O(2) consumption for 1 h. Pre- and postheparin blood samples were taken before exercise (baseline) and at 4, 8, 12, and 24 h after exercise. There was no group difference in LPLa (P > 0.05) over the time points. When the LPLa data from the two groups were combined, LPLa at 24 h after exercise was higher than baseline or at 4, 8, 12 h after exercise (P < 0.05). Plasma TG and lecithin-cholesterol acyltransferase activity (LCATa) were higher in HTG than in NTG, and the total high-density lipoprotein-cholesterol (HDL(tot)-Chol) was lower in HTG than in NTG (P < 0.05). HDL(2)-Chol, LCATa, and cholesterol ester transfer protein activity did not differ during the 24-h postexercise period (P > 0.05). These results suggest that LPLa is still increasing 24 h after an acute aerobic exercise and that the magnitude of the increase in exercise-induced LPLa in HTG was similar to that in NTG. Furthermore, in the sedentary population with or without HTG, the variables related to RCT do not change during the 24-h period after exercise.

Adult↗

PubMed2002

Increased atherosclerosis in diabetic dyslipidemic swine: protection by atorvastatin involves decreased VLDL triglycerides but minimal effects on the lipoprotein profile.

Male Yucatan swine were allocated to four groups (n = 5-6 pigs per group): low fat (3%) fed control, high fat/2% cholesterol (CH) fed (HF), high fat/CH fed with alloxan-induced diabetes (DF) and DF pigs that were treated with atorvastatin (80 mg/day; DF+A). Pigs were fed two meals per day and daily insulin injections were used in diabetic pigs to maintain plasma glucose between 250 and 350 mg/dl. Diabetic dyslipidemic (DF) pigs exhibited greater coronary atherosclerosis and increased collagen deposition in internal mammary artery compared with normoglycemic hyperlipidemic pigs. Although total and LDL CH concentrations did not differ, triglyceride (TG) were increased in DF pigs and FPLC analysis indicated that the LDL/HDL CH ratio was significantly increased in DF compared with HF pigs. The LDL fraction of DF pigs contained larger, lipid enriched particles resembling IDL. Consumption of the high fat/CH diet caused a moderate increase in the percentage of 14:0 fatty acids in plasma lipids and this was compensated by small-moderate declines in several unsaturated fatty acids. There was a significant increase in phospholipid arachidonic acid in DF compared with HF pigs. Atorvastatin protected diabetic pigs from atherosclerosis and decreased total and VLDL TG, but exerted minimal effects on the FPLC lipoprotein and plasma fatty acid profiles and plasma concentrations of total and LDL CH, vitamin A, vitamin E, and lysophosphatidylcholine. Across all groups the plasma CH concentration was positively correlated with hepatic CH concentration. These findings suggest that atorvastatin's protection against coronary artery atherosclerosis in diabetes may involve effects on plasma VLDL TG concentration. Lack of major effects on other lipid parameters, including the LDL/HDL ratio, suggests that atorvastatin may have yet other anti-atherogenic effects, possibly directly in the vessel wall.

Animals↗